What is Acute Respiratory Distress Syndrome (ARDS)?

Acute Respiratory Distress Syndrome (ARDS) is a severe lung condition characterized by rapid onset of widespread inflammation in the lungs, leading to fluid buildup in the air sacs (alveoli). This fluid accumulation makes it difficult for oxygen to reach the bloodstream, resulting in severe oxygen deprivation throughout the body.


The main features of ARDS include:


  • Difficulty Breathing: ARDS typically causes severe shortness of breath, rapid breathing, and low blood oxygen levels (hypoxemia). Individuals with ARDS may feel like they’re suffocating or gasping for air.


  • Rapid Onset: ARDS usually develops rapidly, often within hours to days after the initial injury or illness that triggers the inflammatory response in the lungs.


  • Widespread Inflammation: The lungs become inflamed due to various underlying causes, such as pneumonia, sepsis, aspiration of stomach contents, trauma, or inhalation of harmful substances. This inflammation damages the delicate lung tissues and impairs their ability to function properly.


  • Decreased Lung Compliance: In ARDS, the lungs become stiff and less compliant, meaning they cannot expand and contract easily during breathing. This reduces the efficiency of gas exchange in the lungs, further worsening oxygenation.


  • Multi-Organ Failure: Severe cases of ARDS can lead to systemic complications and multi-organ failure due to inadequate oxygen delivery to vital organs, such as the brain, heart, and kidneys.


What is the relationship between ARDS and oxidative stress?

Acute Respiratory Distress Syndrome (ARDS) involves a complex cascade of inflammatory responses in the lungs, which can lead to oxidative stress. During ARDS, the lungs experience significant oxidative stress due to various factors, including the release of inflammatory mediators, activation of immune cells, and tissue damage.


  • Inflammatory Response: ARDS is characterized by widespread inflammation in the lungs, triggered by various insults such as infection, trauma, or aspiration. This inflammatory response leads to the activation of immune cells like neutrophils and macrophages, which produce reactive oxygen species (ROS) as part of their defense mechanism against pathogens. However, excessive ROS production can overwhelm the antioxidant defense systems in the lungs, leading to oxidative stress.


  • Tissue Damage: The inflammatory process in ARDS damages the delicate lung tissues, including the alveoli and capillaries. This damage disrupts the normal functioning of cells and compromises the integrity of the lung barrier. As a result, there is an increased production of ROS from damaged cells and mitochondria, contributing to oxidative stress.


  • Ischemia-Reperfusion Injury: In ARDS, blood flow to certain areas of the lungs may be compromised, leading to ischemia (lack of oxygen). When blood flow is restored (reperfusion), it can exacerbate oxidative stress through the generation of ROS. This phenomenon, known as ischemia-reperfusion injury, contributes to tissue damage and inflammation in the lungs.


  • Antioxidant Defense System: The lungs possess antioxidant defense mechanisms to counteract oxidative stress, including enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase, as well as non-enzymatic antioxidants like glutathione and vitamins C and E. However, in ARDS, the antioxidant capacity may be overwhelmed by the excessive production of ROS, leading to oxidative damage.


Overall, oxidative stress plays a significant role in the pathogenesis of ARDS by contributing to lung injury, inflammation, and impaired gas exchange.